INACTIVATION OR ELIMINATION OF POTENTIALLY TRYPANOLYTIC, COMPLEMENT-ACTIVATING IMMUNE-COMPLEXES BY PATHOGENIC TRYPANOSOMES
INACTIVATION OR ELIMINATION OF POTENTIALLY TRYPANOLYTIC, COMPLEMENT-ACTIVATING IMMUNE-COMPLEXES BY PATHOGENIC TRYPANOSOMES
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DOI：
10.1128/iai.24.3.617-627.1979
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发表时间：
1979-01-01
影响因子：
3.1
通讯作者：
PROIA, RL
中科院分区：
文献类型：
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作者：
BALBER, AE;BANGS, JD;PROIA, RL
布鲁氏锥虫和贡氏锥虫在同源抗体[Ab]中于0℃孵育30min后，加入豚鼠补体[C]裂解。锥虫在37℃的抗体中孵育。C处理前C组保持不变。含吸附抗体的寄生虫在37℃孵育后仍保持完好。C先于C处理。C处理后存活的细胞比例随着抗体浓度的增加而降低。在C处理后存活的寄生虫继续表达抗原[Ag]，该抗原可以结合C激活抗体，但不携带C激活免疫复合体。布氏毛滴虫种群中几乎所有的细胞都暴露在37度的抗体中。C，但在C处理前暴露于0℃抗体的人群中，只有10-3到10-5的细胞对X-射线照射的小鼠保持感染。只有10-6~10-7的布氏毛滴虫种群暴露于0度抗体。或37度。C治疗前C感染同源抗原免疫的小鼠。从感染抗体和C处理的小鼠中分离的布鲁氏毛滴虫亚株和种群的血清型分析表明，变异型特异性抗原参与了锥虫的溶解，在C处理后存活的布氏毛滴虫可能发生抗原变异。锥虫可能灭活或消除表面免疫复合体的机制以及这一现象在锥虫病中的可能意义进行了讨论。
Trypanosoma brucei brucei and T. congolense incubated in homologous antibody [Ab] at 0.degree.C for 30 min were lysed by subsequent addition of guinea pig complement [C]. Trypanosomes incubated in Ab at 37.degree. C before C treatment remained intact. Parasites bearing adsorbed Ab remained intact when incubated at 37.degree. C before C treatment. The proportion of cells which survived C treatment decreased with increasing Ab concentration. Parasites which survived C treatment continued to express antigens [Ag] which could bind C-activating Ab but did not bear C-activating immune complexes. Virtually all cells in T. brucei populations exposed to Ab at 37.degree. C, but only 10-3 to 10-5 of the cells in populations exposed to Ab at 0.degree.C before C treatment remained infective for X-irradiated mice. Only 10-6 to 10-7 of T. brucei populations exposed to Ab at 0.degree. or 37.degree. C before C treatment infected mice immunized with homologous Ag. Serotype analysis of substrains and of T. brucei populations isolated from mice infected with Ab and C-treated parasites suggested that variant-specific Ag participated in trypanolysis and that T. brucei which survived C treatment could undergo antigenic variation. Mechanisms by which trypanosomes may inactivate or eliminate surface immune complexes and the possible significance of this phenomenon in trypanosomiasis are discussed.